Method and device for providing anti-tachyarrhythmia therapy

ABSTRACT

Various system embodiments comprise at least one sensor input adapted to receive at least one sensed signal associated with a tachyarrhythmia, a feature set extractor adapted to extract at least two features from the at least one sensed signal associated with the tachyarrhythmia, a feature set generator adapted to form a feature set using the at least two features extracted by the feature set extractor, at least one generator adapted for use to selectively apply an anti-tachycardia pacing (ATP) therapy and a neural stimulation (NS) therapy, and a controller adapted to respond to the feature set. The controller is adapted to initiate the NS therapy when the feature set corresponds to criteria for applying the NS therapy to modify the tachyarrhythmia, and initiate the ATP therapy to terminate the modified tachyarrhythmia. Other aspects and embodiments are provided herein.

FIELD OF THE INVENTION

This application relates generally to the treatment of heart diseaseand, more particularly, to systems, devices and methods to treat cardiacarrhythmias with electrical stimulation.

BACKGROUND

The heart is the center of a person's circulatory system. The leftportions of the heart draw oxygenated blood from the lungs and pump itto the organs of the body to provide the organs with their metabolicneeds for oxygen. The right portions of the heart draw deoxygenatedblood from the body organs and pump it to the lungs where the blood getsoxygenated. Contractions of the myocardium provide these pumpingfunctions. In a normal heart, the sinoatrial node, the heart's naturalpacemaker, generates electrical impulses that propagate through anelectrical conduction system to various regions of the heart to excitethe myocardial tissues of these regions. Coordinated delays in thepropagations of the electrical impulses in a normal electricalconduction system cause the various portions of the heart to contract insynchrony, which efficiently pumps the blood. Blocked or abnormalelectrical conduction or deteriorated myocardial tissue causesdysynchronous contraction of the heart, resulting in poor hemodynamicperformance, including a diminished blood supply to the heart and therest of the body. Heart failure occurs when the heart fails to pumpenough blood to meet the body's metabolic needs.

Tachyarrhythmias are abnormal heart rhythms characterized by a rapidheart rate. Examples of tachyarrhythmias include supraventriculartachycardias (SVT's) such as atrial tachycardia (AT), and atrialfibrillation (AF), and the more dangerous ventricular tachyarrhythmiaswhich include ventricular tachycardia (VT) and ventricular fibrillation(VF). Abnormal ventricular rhythms occur when re-entry of a depolarizingwavefront in areas of the ventricular myocardium with differentconduction characteristics becomes self-sustaining or when an excitatoryfocus in the ventricle usurps control of the heart rate from thesinoatrial node. The result is rapid and ineffective contraction of theventricles out of electromechanical synchrony with the atria. Mostabnormal ventricular rhythms exhibit an abnormal QRS complex in anelectrocardiogram because the depolarization spreads from the excitatoryfocus or point of re-entry directly into the myocardium rather thanthrough the normal ventricular conduction system. Ventriculartachycardia is typically characterized by distorted QRS complexes thatoccur at a rapid rate, while ventricular fibrillation is diagnosed whenthe ventricle depolarizes in a chaotic fashion with no identifiable QRScomplexes. Both ventricular tachycardia and ventricular fibrillation arehemodynamically compromising, and both can be life-threatening.Ventricular fibrillation, however, causes circulatory arrest withinseconds and is the most common cause of sudden cardiac death.

Cardioversion, an electrical shock delivered to the heart synchronouslywith the QRS complex, and defibrillation, an electrical shock deliveredwithout synchronization to the QRS complex, can be used to terminatemost tachyarrhythmias. The electric shock terminates the tachyarrhythmiaby simultaneously depolarizing the myocardium and rendering itrefractory. A class of cardiac rhythm management (CRM) devices known asan implantable cardioverter defibrillator (ICD) provides this kind oftherapy by delivering a shock pulse to the heart when the device detectstachyarrhythmias. Another type of electrical therapy for tachycardia isanti-tachycardia pacing (ATP). In ventricular ATP, the ventricles arecompetitively paced with one or more pacing pulses in an effort tointerrupt the reentrant circuit causing the tachycardia. Modem ICDstypically have ATP capability, and deliver ATP therapy or a shock pulsewhen a tachyarrhythmia is detected.

Cardioversion/defibrillation consumes a relatively large amount ofstored power from the battery and can cause patient discomfort. It isdesirable, therefore, to terminate a tachyarrhythmia whenever possiblewithout using shock therapy. Devices have therefore been programmed touse ATP to treat lower rate tachycardias and to usecardioversion/defibrillation shocks to terminate fibrillation andcertain high rate tachycardias.

SUMMARY

Described herein is a device, system and method for treating atrial orventricular tachyarrhythmias which, in addition to ATP and shocktherapy, employs neural stimulation. The neural stimulation may beparasympathetic stimulation or sympathetic inhibition.

Various aspects of the present subject matter relate to a system.Various system embodiments comprise at least one sensor input adapted toreceive at least one sensed signal associated with a tachyarrhythmia, afeature set extractor adapted to extract at least two features from theat least one sensed signal associated with the tachyarrhythmia, afeature set generator adapted to form a feature set using the at leasttwo features extracted by the feature set extractor, at least onegenerator adapted for use to selectively apply an anti-tachycardiapacing (ATP) therapy and a neural stimulation (NS) therapy, and acontroller adapted to respond to the feature set. The controller isadapted to initiate the NS therapy when the feature set corresponds tocriteria for applying the NS therapy to modify the tachyarrhythmia, andinitiate the ATP therapy to terminate the modified tachyarrhythmia.

Various system embodiments comprise at least one sensor input adapted toreceive at least one sensed signal associated with a tachyarrhythmia, afeature set extractor adapted to extract at least two features from theat least one sensed signal associated with the tachyarrhythmia, afeature set generator adapted to form a feature set using the at leasttwo features extracted by the feature set extractor, at least onegenerator adapted for use to selectively apply a shock therapy, an ATPtherapy, and a neural stimulation therapy, and a controller adapted torespond to the feature set. The controller is adapted to initiate theshock therapy when the feature set corresponds to criteria for applyingthe shock therapy, initiate the ATP therapy when the feature setcorresponds to criteria for applying the ATP therapy, and initiate theNS therapy when the feature set corresponds to criteria for applying theNS therapy.

Various aspects of the present subject matter relate to a method.According to various embodiments of the method, a NS therapy is appliedto modify a ventricular tachycardia (VT), and an ATP therapy is appliedto terminate the modified VT.

According to various embodiments of the method, at least one sensedsignal associated with a tachyarrhythmia is received, at least twofeatures are extracted from the at least one sensed signal associatedwith the tachyarrhythmia and a feature set is formed using the at leasttwo features. A shock therapy is provided when the feature setcorresponds to criteria for applying the shock therapy. An ATP therapyis provided when the feature set corresponds to criteria for applyingthe ATP therapy. An NS therapy is provided when the feature setcorresponds to criteria for applying the NS therapy to modify thetachyarrhythmia to be amenable to the ATP therapy.

This Summary is an overview of some of the teachings of the presentapplication and not intended to be an exclusive or exhaustive treatmentof the present subject matter. Further details about the present subjectmatter are found in the detailed description and appended claims. Otheraspects will be apparent to persons skilled in the art upon reading andunderstanding the following detailed description and viewing thedrawings that form a part thereof, each of which are not to be taken ina limiting sense. The scope of the present invention is defined by theappended claims and their equivalents.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 illustrates an anti-tachycardia therapy, according to variousembodiments of the present subject matter.

FIG. 2 illustrates a neural stimulator, and further illustrates variousneural stimulation parameters that can be adjusted to adjust a neuralstimulation therapy, according to various embodiments of the presentsubject matter.

FIG. 3 illustrates an anti-tachycardia therapy, according to variousembodiments of the present subject matter.

FIG. 4 illustrates an implantable medical device, according to variousembodiments of the present subject matter.

FIG. 5 illustrates criteria for use in determining whether to deliver ashock therapy, an anti-tachycardia pacing (ATP) therapy, or an ATPtherapy with neural stimulation to precondition the arrhythmia,according to various embodiments of the present subject matter.

FIG. 6 illustrates an implantable medical device (IMD) having a neuralstimulation (NS) component and cardiac rhythm management (CRM)component, according to various embodiments of the present subjectmatter.

FIG. 7 shows a system diagram of an embodiment of a microprocessor-basedimplantable device, according to various embodiments.

FIG. 8 illustrates a system including an implantable medical device (ND)and an external system or device, according to various embodiments ofthe present subject matter.

FIG. 9 illustrates a system including an external device, an implantableneural stimulator (NS) device and an implantable cardiac rhythmmanagement (CRM) device, according to various embodiments of the presentsubject matter.

FIG. 10 illustrates an IMD placed subcutaneously or submuscularly in apatient's chest with lead(s) positioned to provide a CRM therapy to aheart, and with lead(s) positioned to stimulate a vagus nerve, by way ofexample and not by way of limitation, according to various embodiments.

FIG. 11 illustrates an HMD with lead(s) positioned to provide a CRMtherapy to a heart, and with satellite transducers positioned tostimulate at least one parasympathetic neural target as part of amyocardium conditioning therapy, according to various embodiments.

FIG. 12 is a block diagram illustrating an embodiment of an externalsystem.

DETAILED DESCRIPTION

The following detailed description of the present subject matter refersto the accompanying drawings which show, by way of illustration,specific aspects and embodiments in which the present subject matter maybe practiced. These embodiments are described in sufficient detail toenable those skilled in the art to practice the present subject matter.Other embodiments may be utilized and structural, logical, andelectrical changes may be made without departing from the scope of thepresent subject matter. References to “an”, “one”, or “various”embodiments in this disclosure are not necessarily to the sameembodiment, and such references contemplate more than one embodiment.The following detailed description is, therefore, not to be taken in alimiting sense, and the scope is defined only by the appended claims,along with the full scope of legal equivalents to which such claims areentitled.

Cardiac rate, contractility, and excitability are known to be modulatedby centrally mediated reflex pathways. Baroreceptors and chemoreceptorsin the heart, great vessels, and lungs, transmit cardiac activitythrough vagal and sympathetic afferent fibers to the central nervoussystem. Activation of sympathetic afferents triggers reflex sympatheticactivation, parasympathetic inhibition, vasoconstriction, andtachycardia. In contrast, parasympathetic activation results inbradycardia, vasodilation, and inhibition of vasopressin release. Amongmany other factors, decreased parasympathetic or vagal tone or increasedsympathetic tone is associated with various arrhythmias genesis,including ventricular tachycardia and atrial fibrillation. In ICDs,efficacy of anti-tachycardia therapy such as ATP is also significantlyaffected by sympathetic/parasympathetic activation. It was reported thatsinus tachycardia preceding VT onset and lack of beta blockersindependently predicted higher ATP failure and acceleration. Thecircadian pattern of ATP success may also suggest that increasedsympathetic activation plays a role in ATP therapy efficacy.

The present disclosure relates to an implantable device with thecapability of sensing the presence of a tachyarrhythmia and terminatingthe arrhythmia with a combination of neural stimulation, ATP, and/orhigh-voltage shocks. Embodiments of the present subject matter directlydetermine the appropriate therapy for the tachyarrhythmia using acomposite set of features associated with the tachyarrhythmia. Thenumber of features in the feature set is at least two featuresassociated with the feature set. For example, various embodiments mapthe tachyarrhythmia to the appropriate therapy using the feature set.

Embodiments of the present subject matter use neural stimulation tocondition the tachyarrhythmia to make it more amenable to ATP therapy.Neural stimulation, in the form of sympathetic inhibition orparasympathetic activation, decreases myocardial excitability andconduction time. The neural stimulation thus changes thecharacterizations of the tachycardia to that treatable by ATP. Asidentified above, ATP has conventionally been used to treat lower ratetachycardias, while shocks have been used to terminate higher ratetachycardias and fibrillation. Embodiments of the present subject matterprovide a method to improve the ATP efficacy on a broader spectrum ofVTs such as those with higher rate and/or not very stable rhythms.According to the present subject matter, neurostimulation (NS) is usedto modify the VT characteristics (e.g. slow down the rate) and restorethe hemodynamic function to some extent (e.g. increase LV filling) whenthe VTs are deemed inappropriate to be treated by immediate ATP. Thispreconditioning of the arrhythmia changes the VT characteristics to makethe VT more amendable to ATP therapy, therefore improving the overallsuccess of ATP on wider array of VTs.

According to an embodiment, a VT is detected (e.g. falling in a ratezone and sustained), and an N-dimensional feature set R is constructed,where R={R₁, R₂, . . . , R_(N)}. Each element R_(i) in the R set is afeature extracted either from electrical signals such as intracardiacEGM, or from the signals recorded by one or more sensors such as anaccelerometer, a pressure sensor, an impedance sensor, and the like. Thefeatures from these sensor signals are measures or estimates of thehemodynamic stability during the VT. The composite features in R arethen mapped to one of the following decisions: “Deliver ATP”; “DeliverShock”; “Deliver NS”. The mapping is implemented as a set of algorithms.

“Deliver NS” is selected if the VT rhythms are characterized bymoderately fast rate and unstable rhythm, and modest hemodynamiccompromise. Electrical pulses are generated by the device and deliveredthrough an NS lead to the vagal nerve in the surface of certain bloodvessel where stimulation electrode is positioned. The appropriate NSparameters can be selected using the feature set. If the VT persistsfollowing MS but modified such that it meets the “Deliver ATP” criteria,ATP is delivered. It is expected that applying NS to precondition thetachyarrhythmia for an ATP therapy will allow the ATP to terminate anumber of VTs that would have been rendered to either shock therapywhich can cause patient discomfort or ATP which could fail or evenaccelerate the rhythm without the NS preconditioning.

Anti-Tachycardia Therapy Embodiments

As provided above, a collected feature set can be mapped to determinewhether to treat the tachycardia with ATP therapy, shock therapy, orneural stimulation. If the mapped feature set indicates that the ATPtherapy is not likely to be successful, embodiments of the presentsubject matter apply neural stimulation (NS) to stimulate theparasympathetic system and/or inhibit the sympathetic system, and thendetermine if the resulting tachycardia is amenable to ATP therapy.

FIG. 1 illustrates an anti-tachycardia therapy, according to variousembodiments of the present subject matter. At 101, neural stimulation isapplied to modify the VT for ATP. It is possible that the neuralstimulation may terminate the VT. Thus, at 102, it is determined whetherthe VT is still present. If it is determined that the VT is stillpresent, it is determined at 103 whether the VT has been modified suchthat the modified VT can be successfully treated with ATP. If it has,the process proceeds to 104 to deliver an ATP therapy to terminate theVT. If the VT has not been modified for ATP, the process proceeds to 105to determine whether a time out has occurred. The time out is a periodof time or a number of neural stimulation attempts to modify the VT forATP therapy. If a time out occurs at 105, the process proceeds to 106 toapply a shock therapy, such as a defibrillation or cardioversiontherapy, to terminate the VT. If a time out has not occurred at 105, theprocess proceeds to 107 to determine whether the neural stimulationparameters should be adjusted. If the NS parameters are not to beadjusted at 107, the process returns to 101 to deliver the neuralstimulation. If the NS parameters are to be adjusted at 107, the processproceeds to adjust the neural stimulation parameters at 108, and thenreturns to 101 to deliver the neural stimulation. As discussed belowwith respect to FIG. 2, NS parameters can be adjusted to adjust theintensity of the neural stimulation therapy.

FIG. 2 illustrates a neural stimulator, and further illustrates variousneural stimulation parameters that can be adjusted to adjust a neuralstimulation therapy, according to various embodiments of the presentsubject matter. According to various embodiments, the neural stimulator209 includes modules to set or adjust any one or any combination of twoor more of the following pulse features delivered to the neuralstimulation electrode(s) or transducer(s): the amplitude 210 of thestimulation pulse, the frequency 211 of the stimulation pulse, the burstfrequency 212 of the pulse, the wave morphology 213 of the pulse, andthe pulse width 214. Examples of neural stimulation electrodes includenerve cuffs, and intravascularly-fed electrodes to transvascularlystimulate a neural target. Examples of neural transducers includeultrasound, magnetic and light transducers used to stimulate a neuraltarget. The illustrated burst frequency pulse feature 212 includes burstduration 215 and duty cycle 216, which can be adjusted as part of aburst frequency pulse feature or can be adjusted separately. Forexample, a burst frequency can refer to the number of bursts per minute.Each of these bursts has a burst duration (an amount of time bursts ofstimulation are provided) and a duty cycle (a ratio of time wherestimulation is provided to total time). Thus, by way of example and notlimitation, six bursts can be delivered during a one minute stimulationtime (burst duration), where the length (pulse width) of each burst isfive seconds and the time period between bursts is five seconds. In thisexample, the burst frequency is six bursts per minute, the stimulationtime or burst duration is 60 seconds, and the duty cycle is 50% ((6bursts×5 sec./burst)/60 seconds). Additionally, the duration of one ormore bursts can be adjusted without reference to any steady burstfrequency. For example, a single stimulation burst of a predeterminedburst duration or a pattern of bursts of predetermined pulse width(s)and burst timing can be provided in response to a sensed signal.Furthermore, the duty cycle can be adjusted by adjusting the number ofbursts and/or adjusting the duration of one or more bursts, withoutrequiring the bursts to be delivered with a steady burst frequency.Examples of wave morphology include a square wave, triangle wave,sinusoidal wave, and waves with desired harmonic components to mimicwhite noise such as is indicative of naturally-occurring baroreflexstimulation.

FIG. 3 illustrates an anti-tachycardia therapy, according to variousembodiments of the present subject matter. At 317, it is determinedwhether a tachycardia is detected. If a tachycardia is detected, theprocess proceeds to 318 where a composite feature set R for VT therapyselection is formed. For example, VT characteristics can be extractedfrom the electrogram (EGM) and hemodynamic sensors. The compositefeatures are mapped to tachycardia therapies. Thus, based on thecomposite feature set R, the process proceeds to deliver ATP therapy at319, deliver shock therapy at 320, or deliver neural stimulation at 321.In the illustrated process, for example, it can be determined at 322whether the composite feature set R meets the criteria for immediateapplication of ATP therapy, and if so deliver ATP therapy at 323. Ifnot, it can be determined at 324 whether the composite feature set Rmeets the criteria for immediately applying a shock, and if so deliverthe shock therapy at 325. If not, it can be determined at 326 whetherthe maximum number of neural stimulation attempts for this tachycardiaepisode has been made, and if so a shock can be delivered at 325. Ifnot, neural stimulation is applied at 327. One of ordinary skill willunderstand, upon reading and comprehending this disclosure, that theorder of these determinations can be varied, such that it is determinedwhether the feature set satisfies the shock criteria before the ATPcriteria. Additionally, one of ordinary skill in the art will understandthat a mapping function can be used to directly deliver ATP at 323 whencertain criteria are met, to directly deliver a shock at 325 when othercriteria are met, and deliver neural stimulation at 321 when yet othercriteria are met. At 328, it is determined whether the tachycardiaepisode continues. If a VT is detected at 329, the process returns to318 to form the composite feature set characteristic of the detected VT.If a VT is not detected at 329, it is determined that the therapy hasbeen successful and the VT episode has been terminated.

Device Embodiments

FIG. 4 illustrates an implantable medical device, according to variousembodiments of the present subject matter. The illustrated device 430includes sensor inputs 431, such as EGM or hemodynamic sensors, forexample. The sensors can be connected to the sensor inputs via leads orwireless channels. The sensors can also be used to determine when atachyarrhythmia is detected. Feature extractor(s) 432 are connected tothe sensor inputs 431, to extract a number of sensed features associatedwith the tachyarrhythmia. By way of example and not limitation, thefeature extractor(s) can detect a heart rate 433, heart rate stability434, morphology irregularity 435 and pressure change 436. A feature setgenerator 437 connected to the feature extractor(s) forms a compositefeature set from the extracted features. A comparator 438 compares thegenerated feature set to feature set criteria 439. The illustratedfeature set criteria includes criteria for applying shock 440, criteriafor applying ATP 441, and criteria for applying neural stimulation tocondition the tachyarrhythmia for ATP therapy 442. A controller 443receives a signal from the comparator 438, and appropriately controls ashock generator 444, an ATP generator 445, and/or a NS generator 446based on the comparison of the generated feature set to the feature setcriteria. The shock generator 444, ATP generator 445 and NS generator446 are connected to a stimulation delivery system 447 for use todeliver the shock therapy, the ATP therapy, and the neural stimulationtherapy. Some of these therapies may use common electrodes, according tovarious embodiments. In some embodiments, these therapies use separateelectrodes.

FIG. 5 illustrates criteria for use in determining whether to deliver ashock therapy, an anti-tachycardia pacing (ATP) therapy, or an ATPtherapy with neural stimulation to precondition the arrhythmia,according to various embodiments of the present subject matter.According to various embodiments, when a VT is detected (e.g. asustained rhythm within a rate zone), an N-dimensional feature set R isconstructed, where R={R₁, R₂, . . . , R_(N)}. Each element R_(i) in theR set is a feature extracted either from electrical signals such as anEGM, or from the signals recorded by one or more sensors such as anaccelerometer, a pressure sensor, an impedance sensor and the like. Thefeatures from these sensor signals are measures or estimates of thehemodynamic stability during the VT. In one embodiment, the R set isconstructed as follows: R={R₁,R₂,R₃,R₄} where R₁ is the atrial orventricular heart rate measured by using the rate-sensing channel in thedevice, R₂ is the stability of the rate computed as the variance of themost recent AA or RR intervals, R₃ is the intracardiac morphologyirregularity computed as the sample entropy of the most recent M beatmorphologies, and R₄ is the intra-ventrical pressure difference from thenormal condition (e.g. during normal sinus control) measured by using adedicated implantable pulmonary arterial pressure sensor.

In some embodiments, the pressure is indirectly estimated using othersensors that measure, for example, transthoracic impedance variation, S1and/or S2 heart sound strength variation, and the like. The compositefeatures in R are mapped to one of the following decisions: “DeliverATP”; “Deliver Shock”; and “Deliver NS”. In various embodiments, themapping is implemented as a set of algorithms in a processor orcontroller. In various embodiments, the mapping is performed using alookup table. In various embodiments, the mapping is performed by logiccircuitry.

When the feature set indicates that the tachyarrhythmia is characterizedby significantly unstable hemodynamics, very fast heart rate, or veryunstable rhythms in both rate and morphology, a shock therapy isdelivered immediately or nearly immediately within the capabilities ofthe system. When the feature set indicates that the tachyarrhythmia ischaracterized by slow and hemodynamically stable monomorphic VTs, an ATPtherapy is delivered immediately or nearly immediately within thecapabilities of the system. Such rhythms are slow and hemodynamicallystable monomorphic VTs. When the feature set indicates that thetachyarrhythmia is characterized by moderately fast rate, unstablerhythm, and modest hemodynamic compromise, a NS therapy is applied.Although the neural stimulation may terminate the tachyarrhythmia, theNS therapy is applied to condition the tachyarrhythmia to reduce therate and increase the stability of the arrhythmia such that the modifiedtachyarrhythmia can be classified as being amendable to ATP therapy, andthe corresponding feature set triggers the ATP therapy. Thus, the VT canbe terminated by a preconditioning NS therapy followed by an ATP therapyrather than shock therapy as it would have been delivered in traditionalICD. In one embodiment, this mapping is implemented as a “rule base”where composite rules are used to make therapy decisions in theN-dimensional feature space.

In various embodiments, for example, shock therapy can be delivered forany of the following conditions: the pressure is less than apredetermined value indicating that the tachyarrhythmia ishemodynamically very unstable; the rate is greater than a predeterminedvalue indicating that the tachyarrhythmia is associated with anextremely high heart rate; and the pressure is within a predeterminedrange of pressures, the rate is within a predetermined range of rates,the stability is higher than a threshold, and the morphology is higherthan a threshold indicating that the tachyarrhythmia is hemodynamicallyunstable, is fast, and has an irregular heart rate and morphology.

In various embodiments, for example, ATP therapy is delivered for any ofthe following conditions: the rate is within a predetermined range, andthe stability is less than a threshold indicating that the tachycardiais a slow and stable VT; the pressure is greater than a threshold andthe rate is less than a threshold indicating a hemodynamically stableand slow VT; and the pressure is greater than a threshold, the heartrate is within a predetermined range and the stability is less than athreshold, and the morphology irregularity is less than a thresholdindicating hemodynamically stable VT with moderate heart rate.

In various embodiments, for example, NS therapy is delivered when thepressure is greater than a threshold, the heart rate is within apredetermined range, and the stability is within a predetermined rangeindicate that the tachyarrhythmia is hemodynamically stable but the rateis fast and unstable.

Various embodiments use a decision fusion method to determine whether toapply shock, ATP or NS therapy. An example of a fusion engine functionis provided by X=ƒ(R₁, R₂, . . . , R_(N)). In one example, R_(i) isdefined such that a larger R_(i) indicates severer condition; and ƒ is alinear function of all R_(i) such that X is the weighted sum of allfeatures R. The weight k is the risk factor. Then, for example, shockcan be delivered if X is greater than a first threshold, ATP therapy canbe delivered if X is less than a second threshold, and NS therapy can bedelivered if X is between the first and second thresholds.

According to some embodiments, a number of NS protocols with differentsettings (such as the frequency, duration, etc.) are preprogrammed andstored in the device. In one embodiment, heart rate variability (HRV) ismonitored before and during VT to determine which NS protocol to usewhen “Deliver NS” decision is made. Standard HRV parameters (e.g. SDANNin time domain, or LF/HF ratio in frequency domain) are quantities todescribe sympathetic/parasympathetic balance. Other methods fordetermining autonomic balance or health, such as heart rate turbulence(HRT) or neural sensors, can be used. A significant autonomic imbalancemay require more aggressive NS therapy. The selection of an appropriateNS protocol can be also based on the time of the day. As VT occurrencefollows a circadian rhythm (significantly higher rate of VT occurrenceand ATP failure happens between 6 a.m. to 12 p.m.), a more aggressive NStherapy can be applied during this period of increased VT risk.

The neural stimulation can be applied to a vagus nerve, a cardiac branchof the vagus nerve, a cardiac fat pad, a baroreceptor site, or to otherneural targets that stimulate the parasympathetic nervous system orinhibit the sympathetic nervous system. The neural stimulation can beapplied using intravascularly-fed electrodes, nerve cuffs, satelliteelectrodes, and other known means for stimulating a neural target.

The application of NS therapy before ATP therapy can be useful interminating a broader spectrum of VTs that would have been shocked inconventional ICDs, due to their fast rate, unstable rhythms, orhemodynamic compromise. The efficacy of painless therapy may be greatlyimproved and the painful shock therapy be reduced.

FIG. 6 illustrates an implantable medical device (IMD) 648 having aneural stimulation (NS) component 649 and cardiac rhythm management(CRM) component 650, according to various embodiments of the presentsubject matter. The illustrated device includes a controller 651 andmemory 652. According to various embodiments, the controller includeshardware, software, or a combination of hardware and software to performthe neural stimulation and CRM functions. For example, the programmedtherapy applications discussed in this disclosure are capable of beingstored as computer-readable instructions embodied in memory and executedby a processor. According to various embodiments, the controllerincludes a processor to execute instructions embedded in memory toperform the neural stimulation and CRM functions. Examples of CRMfunctions include bradycardia pacing, anti-tachycardia therapies such asATP, defibrillation and cardioversion, and CRT. The controller alsoexecutes instructions to detect a tachyarrhythmia. The illustrateddevice further includes a transceiver 653 and associated circuitry foruse to communicate with a programmer or another external or internaldevice. Various embodiments include a telemetry coil.

The CRM therapy section 650 includes components, under the control ofthe controller, to stimulate a heart and/or sense cardiac signals usingone or more electrodes. The illustrated CRM therapy section includes apulse generator 654 for use to provide an electrical signal through anelectrode to stimulate a heart, and further includes sense circuitry 655to detect and process sensed cardiac signals. An interface 656 isgenerally illustrated for use to communicate between the controller 651and the pulse generator 654 and sense circuitry 655. Three electrodesare illustrated as an example for use to provide CRM therapy. However,the present subject matter is not limited to a particular number ofelectrode sites. Each electrode may include its own pulse generator andsense circuitry. However, the present subject matter is not so limited.The pulse generating and sensing functions can be multiplexed tofunction with multiple electrodes.

The NS therapy section 649 includes components, under the control of thecontroller, to stimulate a neural stimulation target and/or senseparameters associated with nerve activity or surrogates of nerveactivity such as blood pressure and respiration. Three interfaces 657are illustrated for use to provide neural stimulation. However, thepresent subject matter is not limited to a particular number interfaces,or to any particular stimulating or sensing functions. Pulse generators658 are used to provide electrical pulses to transducer or transducersfor use to stimulate a neural stimulation target. According to variousembodiments, the pulse generator includes circuitry to set, and in someembodiments change, the amplitude of the stimulation pulse, thefrequency of the stimulation pulse, the burst frequency of the pulse,and the morphology of the pulse such as a square wave, triangle wave,sinusoidal wave, and waves with desired harmonic components to mimicwhite noise or other signals. Sense circuits 659 are used to detect andprocess signals from a sensor, such as a sensor of nerve activity, bloodpressure, respiration, and the like. The interfaces 657 are generallyillustrated for use to communicate between the controller 651 and thepulse generator 658 and sense circuitry 659. Each interface, forexample, may be used to control a separate lead. Various embodiments ofthe NS therapy section only includes a pulse generator to stimulateneural targets such a vagus nerve.

FIG. 7 shows a system diagram of an embodiment of a microprocessor-basedimplantable device, according to various embodiments. The controller ofthe device is a microprocessor 760 which communicates with a memory 761via a bidirectional data bus. The controller could be implemented byother types of logic circuitry (e.g., discrete components orprogrammable logic arrays) using a state machine type of design, but amicroprocessor-based system is preferable. As used herein, the term“circuitry” should be taken to refer to either discrete logic circuitryor to the programming of a microprocessor. Shown in the figure are threeexamples of sensing and pacing channels designated “A” through “C”comprising bipolar leads with ring electrodes 762A-C and tip electrodes763A-C, sensing amplifiers 764A-C, pulse generators 765A-C, and channelinterfaces 766A-C. Each channel thus includes a pacing channel made upof the pulse generator connected to the electrode and a sensing channelmade up of the sense amplifier connected to the electrode. The channelinterfaces 766A-C communicate bidirectionally with microprocessor 760,and each interface may include analog-to-digital converters fordigitizing sensing signal inputs from the sensing amplifiers andregisters that can be written to by the microprocessor in order tooutput pacing pulses, change the pacing pulse amplitude, and adjust thegain and threshold values for the sensing amplifiers. The sensingcircuitry of the pacemaker detects a chamber sense, either an atrialsense or ventricular sense, when an electrogram signal (i.e., a voltagesensed by an electrode representing cardiac electrical activity)generated by a particular channel exceeds a specified detectionthreshold. Pacing algorithms used in particular pacing modes employ suchsenses to trigger or inhibit pacing. The intrinsic atrial and/orventricular rates can be measured by measuring the time intervalsbetween atrial and ventricular senses, respectively, and used to detectatrial and ventricular tachyarrhythmias.

The electrodes of each bipolar lead are connected via conductors withinthe lead to a switching network 767 controlled by the microprocessor.The switching network is used to switch the electrodes to the input of asense amplifier in order to detect intrinsic cardiac activity and to theoutput of a pulse generator in order to deliver a pacing pulse. Theswitching network also enables the device to sense or pace either in abipolar mode using both the ring and tip electrodes of a lead or in aunipolar mode using only one of the electrodes of the lead with thedevice housing (can) 768 or an electrode on another lead serving as aground electrode. A shock pulse generator 769 is also interfaced to thecontroller for delivering a defibrillation shock via a pair of shockelectrodes 770 and 771 to the atria or ventricles upon detection of ashockable tachyarrhythmia.

The controller may be programmed with a plurality of selectable ATPpacing protocols that define the manner in which anti-tachycardia pacingis delivered. In a microprocessor-based device, the output of pacingpulses can be controlled by a pacing routine that implements theselected pacing protocol as defined by various parameters. A datastructure stored in memory contains the parameter sets that define eachof the available pacing protocols. Different protocols are apt to bemore successful than others in terminating particular tachyarrhythmiasthat may differ as to rate and/or depolarization pattern. For thisreason, modern cardiac rhythm management devices are capable ofemploying a number of different ATP protocols to deliver therapy.

Neural stimulation channels, identified as channels D and E, areincorporated into the device for delivering parasympathetic stimulationand/or sympathetic inhibition, where one channel includes a bipolar leadwith a first electrode 772D and a second electrode 773D, a pulsegenerator 774D, and a channel interface 775D, and the other channelincludes a bipolar lead with a first electrode 772E and a secondelectrode 773E, a pulse generator 774E, and a channel interface 775E.Other embodiments may use unipolar leads in which case the neuralstimulation pulses are referenced to the can or another electrode. Thepulse generator for each channel outputs a train of neural stimulationpulses which may be varied by the controller as to amplitude, frequency,duty-cycle, and the like. In this embodiment, each of the neuralstimulation channels uses a lead which can be intravascularly disposednear an appropriate stimulation site, e.g., near a baroreceptor in thecase of a sympathetic inhibition channel or near a parasympathetic nervein the case of a parasympathetic stimulation channel. Other types ofleads and/or electrodes may also be employed. A nerve cuff electrode maybe used in place of an intravascularly disposed electrode to provideneural stimulation, where the electrode may be placed, for example,around the cervical vagus nerve bundle to provide parasympatheticstimulation or around the aortic or carotid sinus nerve to providesympathetic inhibition. Baroreceptors in or near the pulmonary arterymay also be stimulated. In another embodiment, the leads of the neuralstimulation electrodes are replaced by wireless links, and theelectrodes for providing parasympathetic stimulation and/or sympatheticinhibition are incorporated into satellite units. Although the appliedneural stimulation may terminate a tachyarrhythmia, the neuralstimulation is expected to change the tachycardia into a rhythm that hasa high likelihood of being successfully terminated by ATP.

The figure illustrates a telemetry interface 776 connected to themicroprocessor, which can be used to communicate with an externaldevice. The illustrated microprocessor 760 is capable of performingneural stimulation therapy routines and myocardial stimulation routines.Examples of NS therapy routines include a pre-ATP NS therapy for atachyarrhythmia. Examples of myocardial therapy routines includebradycardia pacing therapies, anti-tachycardia shock therapies such ascardioversion or defibrillation therapies, anti-tachycardia pacingtherapies, and cardiac resynchronization therapies.

System Embodiments

FIG. 8 illustrates a system 877 including an implantable medical device(IMD) 878 and an external system or device 879, according to variousembodiments of the present subject matter. Various embodiments of theIMD 878 include a combination of NS and CRM functions. The IMD may alsodeliver biological agents and pharmaceutical agents. The external system879 and the IMD 878 are capable of wirelessly communicating data andinstructions. In various embodiments, for example, the external systemand IMD use telemetry coils to wirelessly communicate data andinstructions. Thus, the programmer can be used to adjust the programmedtherapy provided by the IMD, and the NMD can report device data (such asbattery and lead resistance) and therapy data (such as sense andstimulation data) to the programmer using radio telemetry, for example.According to various embodiments, the NMD stimulates a neural targetand/or myocardium to provide an anti-tachycardia therapy.

The external system allows a user such as a physician or other caregiveror a patient to control the operation of IMD and obtain informationacquired by the ND. In one embodiment, external system includes aprogrammer communicating with the IMD bi-directionally via a telemetrylink. In another embodiment, the external system is a patient managementsystem including an external device communicating with a remote devicethrough a telecommunication network. The external device is within thevicinity of the IMD and communicates with the ND bi-directionally via atelemetry link. The remote device allows the user to monitor and treat apatient from a distant location. The patient monitoring system isfurther discussed below.

The telemetry link provides for data transmission from implantablemedical device to external system. This includes, for example,transmitting real-time physiological data acquired by IMD, extractingphysiological data acquired by and stored in IMD, extracting therapyhistory data stored in implantable medical device, and extracting dataindicating an operational status of the IMD (e.g., battery status andlead impedance). Telemetry link also provides for data transmission fromexternal system to IMD. This includes, for example, programming the IMDto acquire physiological data, programming IMD to perform at least oneself-diagnostic test (such as for a device operational status), andprogramming the IMD to deliver at least one therapy.

FIG. 9 illustrates a system 977 including an external device 979, animplantable neural stimulator (NS) device 980 and an implantable cardiacrhythm management (CRM) device 981, according to various embodiments ofthe present subject matter. Various aspects involve a method forcommunicating between an NS device and a CRM device or other cardiacstimulator. In various embodiments, this communication allows one of thedevices 980 or 981 to deliver more appropriate therapy (i.e. moreappropriate NS therapy or CRM therapy) based on data received from theother device. Some embodiments provide on-demand communications. Invarious embodiments, this communication allows each of the devices todeliver more appropriate therapy (i.e. more appropriate NS therapy andCRM therapy) based on data received from the other device. Theillustrated NS device and the CRM device are capable of wirelesslycommunicating with each other, and the external system is capable ofwirelessly communicating with at least one of the NS and the CRMdevices. For example, various embodiments use telemetry coils towirelessly communicate data and instructions to each other. In otherembodiments, communication of data and/or energy is by ultrasonic means.Rather than providing wireless communication between the NS and CRMdevices, various embodiments provide a communication cable or wire, suchas an intravenously-fed lead, for use to communicate between the NSdevice and the CRM device. In some embodiments, the external systemfunctions as a communication bridge between the NS and CRM devices.

FIG. 10 illustrates an IMD 1082 placed subcutaneously or submuscularlyin a patient's chest with lead(s) 1083 positioned to provide a CRMtherapy to a heart, and with lead(s) 1084 positioned to stimulate avagus nerve, by way of example and not by way of limitation, accordingto various embodiments. The leads 1083 can be used to deliver ATP and/orshock therapy. According to various embodiments, the leads 1083 arepositioned in or proximate to the heart to provide a desired cardiacpacing therapy. In some embodiments, the lead(s) 1083 are positioned inor proximate to the heart to provide a desired CRT therapy. Someembodiments place the leads in positions with respect to the heart thatenable the lead(s) to deliver the combinations of at least two of thepacing, defibrillation and CRT therapies. According to variousembodiments, neural stimulation lead(s) 1084 are subcutaneously tunneledto a neural target, and can have a nerve cuff electrode to stimulate theneural target. Some lead embodiments are intravascularly fed into avessel proximate to the neural target, and use transducer(s) within thevessel to transvascularly stimulate the neural target. For example, someembodiments stimulate the vagus nerve using electrode(s) positionedwithin the internal jugular vein.

FIG. 11 illustrates an IMD 1182 with lead(s) 1183 positioned to providea CRM therapy to a heart, and with satellite transducers 1184 positionedto stimulate at least one parasympathetic neural target as part of amyocardium conditioning therapy, according to various embodiments. Thesatellite transducers are connected to the IMD, which functions as theplanet for the satellites, via a wireless link. Stimulation andcommunication can be performed through the wireless link. Examples ofwireless links include RF links and ultrasound links. Although notillustrated, some embodiments perform myocardial stimulation usingwireless links. Examples of satellite transducers include subcutaneoustransducers, nerve cuff transducers and intravascular transducers.

FIG. 12 is a block diagram illustrating an embodiment of an externalsystem 1285. The external system includes a programmer, in someembodiments. In the embodiment illustrated in FIG. 12, the externalsystem includes a patient management system. As illustrated, externalsystem 1285 is a patient management system including an external device1286, a telecommunication network 1287, and a remote device 1288.External device 1286 is placed within the vicinity of an IMD andincludes external telemetry system 1289 to communicate with the IMD.Remote device(s) 1288 is in one or more remote locations andcommunicates with external device 1286 through network 1287, thusallowing a physician or other caregiver to monitor and treat a patientfrom a distant location and/or allowing access to various treatmentresources from the one or more remote locations. The illustrated remotedevice 1288 includes a user interface 1290.

One of ordinary skill in the art will understand that, the modules andother circuitry shown and described herein can be implemented usingsoftware, hardware, and combinations of software and hardware. As such,the term module is intended to encompass software implementations,hardware implementations, and software and hardware implementations.

The methods illustrated in this disclosure are not intended to beexclusive of other methods within the scope of the present subjectmatter. Those of ordinary skill in the art will understand, upon readingand comprehending this disclosure, other methods within the scope of thepresent subject matter. The above-identified embodiments, and portionsof the illustrated embodiments, are not necessarily mutually exclusive.These embodiments, or portions thereof, can be combined. In variousembodiments, the methods provided above are implemented as a computerdata signal embodied in a carrier wave or propagated signal, thatrepresents a sequence of instructions which, when executed by aprocessor cause the processor to perform the respective method. Invarious embodiments, methods provided above are implemented as a set ofinstructions contained on a computer-accessible medium capable ofdirecting a processor to perform the respective method. In variousembodiments, the medium is a magnetic medium, an electronic medium, oran optical medium.

Although specific embodiments have been illustrated and describedherein, it will be appreciated by those of ordinary skill in the artthat any arrangement which is calculated to achieve the same purpose maybe substituted for the specific embodiment shown. This application isintended to cover adaptations or variations of the present subjectmatter. It is to be understood that the above description is intended tobe illustrative, and not restrictive. Combinations of the aboveembodiments as well as combinations of portions of the above embodimentsin other embodiments will be apparent to those of skill in the art uponreviewing the above description. The scope of the present subject mattershould be determined with reference to the appended claims, along withthe full scope of equivalents to which such claims are entitled.

1. A system, comprising: at least one sensor input adapted to receive atleast one sensed signal associated with a tachyarrhythmia; a feature setextractor adapted to extract at least two features from the at least onesensed signal associated with the tachyarrhythmia; a feature setgenerator adapted to form a feature set using the at least two featuresextracted by the feature set extractor; at least one generator adaptedfor use to selectively apply an anti-tachycardia pacing (ATP) therapy,and a neural stimulation therapy (NS therapy); and a controller adaptedto respond to the feature set, the controller being adapted to: detect aventricular tachycardia (VT); use the feature set generator to constructthe feature set in response to the detected VT; initiate the NS therapywhen the feature set corresponds to criteria for applying the NS therapyto modify the detected VT and facilitate successful ATP therapy, whereinthe NS therapy is initiated to modify the detected VT when the detectedVT is characterized by a moderately fast rate, an unstable rhythm and amodest hemodynamic compromise; and initiate the ATP therapy to terminatethe modified VT.
 2. The system of claim 1, wherein the at least onesensor input includes an input to receive an electrogram (EGM) signal.3. The system of claim 1, wherein the at least one sensor input includesan input to receive a signal from a hemodynamic sensor.
 4. The system ofclaim 1, wherein the at least two features are selected from a heartrate, a stability of the heart rate, an irregularity of an electrogrammorphology, or a pressure.
 5. The system of claim 4, wherein thepressure, the heart rate and the heart rate stability indicates that thetachyarrhythmia is hemodynamically stable but the heart rate is fast andunstable.
 6. The system of claim 4, wherein the criteria for applyingthe NS therapy to modify the detected VT includes: the pressure ishigher than a first pressure threshold, the heart rate is higher than afirst heart rate threshold and lower than a second heart rate threshold,and the heart rate stability is higher than a first threshold and lowerthan a second threshold.
 7. The system of claim 1, wherein the at leastone generator is incorporated in a housing of a single implantablemedical device.
 8. The system of claim 1, wherein the at least onegenerator includes a first generator incorporated in a housing of afirst implantable medical device, and a second generator incorporated ina housing of a second implantable medical device.
 9. The system of claim1, further comprising at least one electrode adapted to stimulate avagus nerve.
 10. The system of claim 9, further comprising anintravascularly-fed electrode adapted for use in transvascularlystimulating the vagus nerve from an internal jugular vein.
 11. Thesystem of claim 9, further comprising a subcutaneously-fed lead nervecuff electrode adapted for use in stimulating the vagus nerve.
 12. Thesystem of claim 1, wherein the controller is adapted to determine if thefeature set for the detected VT represents a slow and hemodynamicallystable monomorphic VT and initiate the ATP therapy to terminate thedetected VT when the feature set for the detected VT represents the slowand hemodynamically stable monomorphic VT.
 13. The system of claim 1,wherein the at least one generator is further adapted for use to apply ashock therapy, the feature set extractor is adapted to extract apressure, the controller is adapted to construct the feature set usingthe pressure extracted by the feature set extractor in response to thedetected VT, and choose the ATP therapy, the NS therapy or the shocktherapy based on the feature set constructed using the pressure.
 14. Thesystem of claim 1, wherein: the at least one generator is furtheradapted for use to apply a shock therapy, the feature set extractor isadapted to extract a heart rate, heart rate stability, morphologyirregularity and pressure; the controller is adapted to construct thefeature set using the heart rate, heart rate stability, morphologyirregularity and pressure, and is further adapted to determine if: theheart rate is in a slow range, fast range, or a middle range between theslow and fast ranges; the heart rate stability is in a stable range, anunstable range, or a middle range between the stable and unstableranges; the morphology irregularity is in a regular range, an irregularrange, or a middle range between the regular and irregular ranges; andthe pressure is in a low range, a high range, or a middle range betweenthe low and high ranges; and the controller is adapted to: deliver theNS therapy followed by the ATP therapy when the pressure is in the highrange, the heart rate is in the middle range, and the heart ratestability is in the middle range; deliver the shock therapy if: thepressure is in the low range, or the heart rate is in the high range, orthe pressure is in the middle range, the heart rate is in the middlerange, the heart rate stability is in the unstable range, and themorphology irregularity is in the irregular range; and deliver the ATPtherapy if: the heart rate is in the low range and the heart ratestability is in the low range; or the pressure is in the high range andthe heart rate is in the low range, or the pressure is in the high rangeand the heart rate is in the middle range and the heart rate stabilityis in the stable range and the morphology irregularity is in the regularrange.
 15. A system, comprising: means for detecting a ventriculartachycardia (VT) and constructing a feature set in response to thedetected VT; means for applying a neural stimulation (NS) therapy tomodify a ventricular tachycardia (VT) and facilitate successfulanti-tachycardia pacing (ATP) therapy, wherein the means for applyingthe NS therapy includes means for initiating the NS therapy when thefeature set corresponds to criteria for applying the NS therapy tomodify the detected VT and facilitate successful ATP therapy, whereinthe NS therapy is initiated to modify the detected VT when the detectedVT is characterized by a moderately fast rate, an unstable rhythm and amodest hemodynamic compromise; and means for applying the ATP therapy toterminate the modified VT, wherein the means for applying the NS therapyto modify the VT includes means for comparing a composite feature setfrom at least one sensed signal associated with the VT until thecomposite feature set indicates that the ATP therapy will be successfulin terminating the modified VT.
 16. The system of claim 15, wherein thecomposite feature set includes at least two features from the at leastone sensed signal, the at least two features being selected from a heartrate, a stability of the heart rate, an irregularity of an electrogrammorphology, or a pressure.
 17. A method, comprising: detecting aventricular tachycardia (VT) and constructing a feature set in responseto the detected VT; applying a neural stimulation (NS) therapy to modifya ventricular tachycardia (VT) and facilitate successfulanti-tachycardia pacing (ATP) therapy, wherein applying the NS therapyincludes initiating the NS therapy when the feature set corresponds tocriteria for applying the NS therapy to modify the detected VT andfacilitate successful ATP therapy, wherein the NS therapy is initiatedto modify the detected VT when the detected VT is characterized by amoderately fast rate, an unstable rhythm and a modest hemodynamiccompromise; determining if the VT has been modified for the ATP therapyafter the NS therapy is applied; and applying the ATP therapy toterminate the modified VT, wherein applying the ATP therapy includesapplying the ATP therapy when it is determined that the VT has beenmodified for the ATP therapy.
 18. The method of claim 17, furthercomprising determining if the VT is still present after the NS therapyis applied, wherein applying the ATP therapy includes applying the ATPtherapy only if the VT remains present after the NS therapy.
 19. Themethod of claim 17, further comprising applying shock therapy when it isdetermined that the NS therapy did not modify the VT to facilitatesuccessful ATP therapy.
 20. The method of claim 19, wherein applyingshock therapy includes applying shock therapy after a time out hasoccurred.
 21. The method of claim 17, further comprising reapplying theNS therapy when it is determined that the NS therapy did not modify theVT to facilitate successful ATP therapy.
 22. The method of claim 21,further comprising adjusting NS therapy parameters before reapplying theNS therapy.
 23. The method of claim 17, wherein applying the NS therapyto modify the VT includes comparing a composite feature set from atleast one sensed signal associated with the VT until sensed signalsassociated with the modified VT has a composite feature set thatindicates that the ATP therapy will be successful in terminating themodified VT.
 24. The method of claim 23, wherein the composite featureset includes at least two features from the at least one sensed signal,the at least two features being selected from a heart rate, a stabilityof the heart rate, an irregularity of an electrogram morphology, or apressure.
 25. A system, comprising: at least one sensor input adapted toreceive at least one sensed signal associated with a tachyarrhythmia; afeature set extractor adapted to extract at least two features from theat least one sensed signal associated with the tachyarrhythmia; afeature set generator adapted to form a feature set using the at leasttwo features extracted by the feature set extractor; at least onegenerator adapted for use to selectively apply an anti-tachycardiapacing (ATP) therapy, and a neural stimulation therapy (NS therapy); anda controller adapted to respond to the feature set, the controller beingadapted to: detect a ventricular tachycardia (VT); use the feature setgenerator to construct the feature set in response to the detected VT;initiate the NS therapy when the feature set corresponds to criteria forapplying the NS therapy to modify the detected VT when the detected VTis characterized by a moderately fast rate, an unstable rhythm and amodest hemodynamic compromise; and initiate the ATP therapy to terminatethe modified VT, wherein: the at least one generator is further adaptedfor use to apply a shock therapy, the feature set extractor is adaptedto extract a pressure, the controller is adapted to construct thefeature set using the pressure extracted by the feature set extractor inresponse to the detected VT, and choose the ATP therapy, the NS therapyor the shock therapy based on the feature set constructed using thepressure; the feature set extractor is further adapted to extract heartrate, heart rate stability, and morphology irregularity; the controlleris adapted to choose the NS therapy when the pressure is greater than athreshold, the heart rate is within a predetermined range, and the heartrate stability is within a predetermined range to indicate that thedetected tachyarrhythmia is hemodynamically stable but the heart rate isfast and unstable; and the controller is adapted to choose the ATPtherapy when: the heart rate is within a predetermined range and theheart rate stability is less than a threshold indicating that thetachycardia is a slow and stable VT; or the pressure is greater than athreshold and the heart rate is less than a threshold indicating ahemodynamically stable and slow VT; or the pressure is greater than athreshold, the heart rate is within a predetermined range and the heartrate stability is less than a threshold; or the morphology irregularityis less than a threshold indicating hemodynamically stable VT withmoderate heart rate.
 26. The system of claim 25, wherein the controlleris adapted to choose the shock therapy when: the pressure is less than apredetermined value indicating that the tachyarrhythmia ishemodynamically very unstable; the heart rate is greater than apredetermined value indicating that the tachyarrhythmia is associatedwith an extremely high heart rate; the pressure is within apredetermined range of pressures, the heart rate is within apredetermined range of rates, the heart rate stability is higher than athreshold and the morphology irregularity is higher than a thresholdindicating that the tachyarrhythmia is hemodynamically unstable, is fastand has an irregular heart rate and morphology.